Department of Biochemistry, University of Wisconsin, Madison, WI 53706, USA.
Proc Natl Acad Sci U S A. 2012 May 29;109(22):8501-4. doi: 10.1073/pnas.1206054109. Epub 2012 May 16.
The development of experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis, has been studied in mice that were (i) vitamin D-deficient, (ii) minus the vitamin D receptor, (iii) minus a vitamin D 25-hydroxylase, and (iv) minus the vitamin D 25-hydroxyvitamin D-1α-hydroxylase. EAE development was markedly suppressed in mice lacking the vitamin D receptor and partially suppressed in vitamin D-insufficient mice. However, the absence of either of the two key hydroxylases (i.e., 25-hydroxylase and 1α-hydroxylase) neither inhibits nor enhances the development of EAE. These results indicate that vitamin D and the vitamin D receptor are required for the development of EAE. The results also suggest that 1,25-dihydroxyvitamin D(3) may not play a role in this autoimmune response.
实验性自身免疫性脑脊髓炎（EAE）的发展，多发性硬化症的一种模型，在以下几种老鼠中被研究：（i）缺乏维生素 D，（ii）缺乏维生素 D 受体，（iii）缺乏维生素 D25-羟化酶，和（iv）缺乏维生素 D25-羟维生素 D-1α-羟化酶。缺乏维生素 D 受体的老鼠的 EAE 发展明显受到抑制，而维生素 D 不足的老鼠则部分受到抑制。然而，这两种关键羟化酶（即 25-羟化酶和 1α-羟化酶）的缺失既不抑制也不增强 EAE 的发展。这些结果表明维生素 D 和维生素 D 受体是 EAE 发展所必需的。这些结果还表明 1,25-二羟维生素 D(3)可能在这种自身免疫反应中不起作用。
